A new meta-analysis discovered that the repletion of vitamin D deficiency may lead to HbA1C reductions among type II diabetes patients.

Diabetes is responsible for over 75,000 deaths each year in the U.S, making it the seventh leading cause of death. Approximately 29.1 million people in the U.S. have diabetes, with type 2 diabetes accounting for about 90 to 95 percent of adult cases.

Type 2 diabetes is a chronic condition, in which the body resists the effects of insulin or doesn’t produce enough insulin to maintain a normal blood sugar level.

Insulin is a hormone made by pancreatic beta cells that regulates the body’s blood sugar level. Insulin secretion into the bloodstream enables sugar to enter the cells. This lowers the amount of sugar in the bloodstream.

Researchers propose that vitamin D may help diabetes by stimulating insulin secretion via the vitamin D receptors in the pancreas, lowering inflammation and thereby improving insulin resistance or improving insulin resistance through the vitamin D receptors in the muscles and liver.

Observational studies have established a clear relationship between low vitamin D levels and diabetes. However, whether vitamin D supplementation improves glycemic control is still up for debate. In an effort to resolve this argument, researchers recently conducted a meta-analysis of 22 randomized controlled trials that assessed the effects of vitamin D supplementation on glucose metabolism, specifically HbA1c and fasting blood glucose. HbA1c is a lab test that shows the average blood sugar (glucose) level over the previous three months.

The meta-analysis revealed that vitamin D supplementation led to a modest, yet significant, reduction in HbA1C compared to placebo (-0.32%, p = 0.022). However, no effect on fasting blood glucose was observed (p = 0.542).

The researchers performed subgroup analyses. They found that higher doses of vitamin D showed no treatment effect on HbA1C; whereas lower doses of vitamin D showed improvements. This finding may be explained by the efficacy of daily dosing versus bolus dosing. While the meta-analysis would calculate a 50,000 IU weekly dose equivalent to about 7,000 IU daily, research shows that it isn’t quite that simple. Bolus dosing likely results in reduced availability of active vitamin D for cells in comparison to daily dosing. Therefore, this effect may weaken the ability of vitamin D to act locally within the pancreas, muscles and liver.

The analysis also discovered more profound reductions of HbA1C in studies that achieved repletion of vitamin D deficiency (p < 0.001). The same was true for fasting blood glucose, but these reductions remained insignificant (p = 0.064).

The researchers concluded,

“We found a modest reduction of 0.32% in HbA1C after vitamin D treatment in individuals with type 2 diabetes…On the other hand, we found no difference in [fasting blood glucose] among adults with type 2 diabetes treated with versus without vitamin D.”

They continued to state,

“We found that the normalization of vitamin D levels may be needed to observe beneficial effects of vitamin D supplementation on glycemic outcomes.”

The meta-analysis made a clear point; one cannot rule out the possibility that vitamin D improves a health outcome until well designed RCTs are conducted, meaning a RCT with a deficient sample population at baseline, a sample population affected by the condition that is being researched and an adequate, daily vitamin D3 dosage. While this criteria for a well-designed RCT may seem obvious, many skeptics fail to consider the criteria when a negative study is published. Of course, a daily 400 IU vitamin D supplement won’t lead to improvements, because it won’t allow a person to achieve sufficiency. If all the participants are sufficient at baseline, how will they reap new benefits from vitamin D? These questions among others must be asked when evaluating studies.

Overall, these findings are encouraging. The meta-analysis did not reveal miraculous results. Instead, the improvements were quite modest. However, 15 of the 22 studies were considered poor quality. The fact that the studies that adhered to the criteria for well-designed RCTs produced the most significant results suggest that vitamin D likely plays a role in type II diabetes.

Further randomized controlled trials of high quality are needed before drawing any definitive conclusions regarding the effects of vitamin D on type II diabetes.